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Article: Oct4 is Epigenetically Regulated by Methylation in Normal Placenta and Gestational Trophoblastic Disease

TitleOct4 is Epigenetically Regulated by Methylation in Normal Placenta and Gestational Trophoblastic Disease
Authors
KeywordsChoriocarcinoma
Gestational trophoblastic disease
Hydatidiform mole
Methylation
Oct4
Placenta
Issue Date2008
PublisherWB Saunders Co Ltd. The Journal's web site is located at http://www.elsevier.com/locate/placenta
Citation
Placenta, 2008, v. 29 n. 6, p. 549-554 How to Cite?
AbstractOct4 is a transcription factor that plays a crucial role in maintaining pluripotency of embryonic stem cells. Down-regulation of Oct4 is associated with the differentiation of trophectoderm cell lineage, from which the normal placenta derives. We investigated the methylation and expression status of Oct4 in normal placenta and gestational trophoblastic disease (GTD) as attempts to investigate the role of Oct4 in the pathogenesis of GTD. By methylation-specific PCR, we observed both methylated and unmethylated Oct4 alleles in all 25 first trimester and 10 term placentas while 33% (18/54) of hydatidiform moles, and two choriocarcinoma cell line (JEG3 and JAR), only displayed methylated Oct4 allele. By quantitative TaqMan real-time PCR, Oct4 mRNA was significantly reduced in hydatidiform moles (P = 0.04), JEG3 and JAR (P = 0.024) when compared with normal placentas. Oct4 methylation was significantly correlated with Oct4 mRNA expression in placenta and GTD (P = 0.012). Hypermethylation in minimal promoter and exon 1 region of Oct4 were confirmed in JEG3 and JAR by bisulfite genomic sequencing. The Oct4 mRNA expression in JEG3 and JAR increased after treatment with 5-aza-2′-deoxycytidine and/or trichostatin A. Our findings suggest that Oct4 is down-regulated by hypermethylation in normal placenta and GTD and such process is important in pathogenesis of GTD. © 2008 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87105
ISSN
2015 Impact Factor: 2.972
2015 SCImago Journal Rankings: 1.608
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, HJen_HK
dc.contributor.authorSiu, MKYen_HK
dc.contributor.authorWong, ESYen_HK
dc.contributor.authorWong, KYen_HK
dc.contributor.authorLi, ASMen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T09:25:23Z-
dc.date.available2010-09-06T09:25:23Z-
dc.date.issued2008en_HK
dc.identifier.citationPlacenta, 2008, v. 29 n. 6, p. 549-554en_HK
dc.identifier.issn0143-4004en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87105-
dc.description.abstractOct4 is a transcription factor that plays a crucial role in maintaining pluripotency of embryonic stem cells. Down-regulation of Oct4 is associated with the differentiation of trophectoderm cell lineage, from which the normal placenta derives. We investigated the methylation and expression status of Oct4 in normal placenta and gestational trophoblastic disease (GTD) as attempts to investigate the role of Oct4 in the pathogenesis of GTD. By methylation-specific PCR, we observed both methylated and unmethylated Oct4 alleles in all 25 first trimester and 10 term placentas while 33% (18/54) of hydatidiform moles, and two choriocarcinoma cell line (JEG3 and JAR), only displayed methylated Oct4 allele. By quantitative TaqMan real-time PCR, Oct4 mRNA was significantly reduced in hydatidiform moles (P = 0.04), JEG3 and JAR (P = 0.024) when compared with normal placentas. Oct4 methylation was significantly correlated with Oct4 mRNA expression in placenta and GTD (P = 0.012). Hypermethylation in minimal promoter and exon 1 region of Oct4 were confirmed in JEG3 and JAR by bisulfite genomic sequencing. The Oct4 mRNA expression in JEG3 and JAR increased after treatment with 5-aza-2′-deoxycytidine and/or trichostatin A. Our findings suggest that Oct4 is down-regulated by hypermethylation in normal placenta and GTD and such process is important in pathogenesis of GTD. © 2008 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co Ltd. The Journal's web site is located at http://www.elsevier.com/locate/placentaen_HK
dc.relation.ispartofPlacentaen_HK
dc.subjectChoriocarcinomaen_HK
dc.subjectGestational trophoblastic diseaseen_HK
dc.subjectHydatidiform moleen_HK
dc.subjectMethylationen_HK
dc.subjectOct4en_HK
dc.subjectPlacentaen_HK
dc.subject.meshAzacitidine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA Modification Methylases - antagonists & inhibitorsen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshEpigenesis, Genetic - physiologyen_HK
dc.subject.meshExonsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - drug effectsen_HK
dc.subject.meshGestational Trophoblastic Disease - genetics - metabolism - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHydroxamic Acids - pharmacologyen_HK
dc.subject.meshOctamer Transcription Factor-3 - genetics - metabolismen_HK
dc.subject.meshPlacenta - metabolism - pathologyen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.titleOct4 is Epigenetically Regulated by Methylation in Normal Placenta and Gestational Trophoblastic Diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-4004&volume=29&issue=6&spage=549&epage=554&date=2008&atitle=Oct4+is+Epigenetically+Regulated+by+Methylation+in+Normal+Placenta+and+Gestational+Trophoblastic+Diseaseen_HK
dc.identifier.emailSiu, MKY: mkysiu@hkucc.hku.hken_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authoritySiu, MKY=rp00275en_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.placenta.2008.03.003en_HK
dc.identifier.pmid18440631-
dc.identifier.scopuseid_2-s2.0-43849107501en_HK
dc.identifier.hkuros145300en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-43849107501&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue6en_HK
dc.identifier.spage549en_HK
dc.identifier.epage554en_HK
dc.identifier.isiWOS:000256831400010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhang, HJ=8597830900en_HK
dc.identifier.scopusauthoridSiu, MKY=24924018400en_HK
dc.identifier.scopusauthoridWong, ESY=23101622300en_HK
dc.identifier.scopusauthoridWong, KY=13310164400en_HK
dc.identifier.scopusauthoridLi, ASM=24076332400en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK

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